Thank you very much. This is Torbjørn Bjerke. I'm the CEO of SynAct Pharma, and welcome and good afternoon to everybody from calling in from from Europe, and good morning to the listeners from from the U.S. The purpose of this call today is really to discuss and talk about the further analysis we have done in the EXPAND study. So it will be an update, and you'll see all the data that we have gathered so far. When we presented the first data a bit more than a week ago, we had all the patients in, and we could unfortunately not show any significance between the placebo and active on the primary readout being the ACR20. So what we did since then until now has really been to dissect the whole study and to go from part to part. And in that work, we also went to an understanding of why do we not look at patients that do have a systemic inflammation? Because after all, resomelagon or AP1189 is an anti-inflammatory drug, and this requires that you do have an inflammation in order to have an effect. So what we then did was to take CRP, the C-reactive protein. We do measure it with high accuracy, and we elucidated the relevance of CRP on efficacy. It's a fact that CRP above three, then you start to have a systemic inflammation. So today we will present to you that resomelagon-treated patients with elevated CRP at baseline, that is more than 3 milligrams per liter, had a consistent responsiveness over placebo at 12 weeks across all outcome measures. And from a drug development point of view, that is important, that not only find it in your primary readout, but you find it across the secondary readouts. And Thomas will show us that and have that discussion. So what we found was that 67.6% of resomelagon-treated patients achieved an ACR20 response, compared to 54.3% on placebo. What we also find is quite interesting is the health assessment questionnaire disability index. That is a component of the ACR scoring system, and that one improved almost three times the minimal clinically important difference. So a very, very relevant finding. So these patients that have elevated CRP, which, as we all know, is a blood marker for systemic inflammation, is extremely relevant population in inflammatory diseases, including RA. We will also show you the improvement that we saw in the CDAI score and DAS28 scoring system, and it really mirrors what we have seen with ACR 20. So what does that mean? So it means that identifying this population is important in helping to understand the EXPAND study and of course, prepare for the release of the RESOLVE-2A study where we went out yesterday saying that about 70% of the RESOLVE-2A patients have CRP more than 3 milligrams per liter. And as we know, that these patients are DMARD-IR, so they have not been responding well to methotrexate treatment. So, we believe the findings today also puts on the future in terms of identifying the most relevant, clinical patients for further, clinical development of resomelagon. And with that introduction, I will hand over to Thomas. Please, Thomas. Well, thank you very much. The first slide here shows on the left, and that would go through all the slides I'll show you. On the left, we have the readouts from the full study, meaning the full population of patients who completed dosing. And to the right, we have the subgroup of patients who had a CRP level of three or higher at baseline. In other words, those patients who had active systemic activation of inflammation, which in many ways is logical that our compound, that is, Torbjørn mentioned, it's anti-inflammatory, but it's on top of that, just as important, has the ability to resolve resolution, meaning to boost pathways that resolve an ongoing inflammation. What we see and what we saw and what we reported last week, that we were not able in the full study to show any, and full data set, to see any any changes in ACR 20 score in patients after 12-week study. You can see here how it developed the ACR score in the full data set. When you then look at the patients with activated systemic inflammation, that's a subset approximately 60, a little more than 60% of the full data of all the patients. You can see here that we have, at all time points, starting here from week four, and then up to, 12 weeks, we have a higher response rate, indicating that the compounds, induce, treatment effects that is, superior to placebo. Unfortunately, it's only a sub-study, and therefore, we, can look at this as numerically higher changes, as they did not reach statistical significance. But a very, very clear, trend here with the, reaching up to more than 70% in these patients. When you then look at the next slides, here, the next slide, we have here the ACR 20, 70, 50, and 70 for the full data set to the left and to the, again, to the, with the subset of patients here with activated systemic inflammation. What you, where we see a very clear indication of increased activity on ACR 20, it did not in this study show to be markedly changed on ACR 50 and 70. Nevertheless, what we know is that most of these parameters, that is a couple of ACR is driving the scoring system. One of those is the HAQ score. As Torbjørn mentioned, HAQ is a health assessment questionnaire disability index for the patients, a measure of the patient's ability to handle normal daily living. And in the full data set, we saw a very early onset. And the more you reduce your index numbers, the better. Based on a scoring system of eight different categories, where the patient then evaluate the ability to handle those from without problems to very, very difficult and not possible at all. And what we saw was that in the placebo group, we had a very early onset of improvements here, but whereas the compound here gradually took over and numerically had a higher response rate after 12 weeks. If we then again go to the patients who had systemic inflammation evaluated by CRP, you can see here that the effect really turns in after 8 weeks and continue here. And after 12 weeks, we had the improvements in the disability index here was 60% better than on placebo treatment. Really indicating that we do have here a potential treatment effects for the benefit of the patients. Torbjørn mentioned in the beginning that it was like this 0.64, that's actually quite a relevant reduction. In normal, and out in the literature, we talk about 0.22 points reduction is a clinically meaningful reduction. So what we have done here is made a small post-hoc analysis, looking at how many patients were actually then qualified for this. And this is shown on this slide here. The percentage of patients reaching minimal clinically important difference in HAQ score over the different time points in the study. And as you can see here, again, to the left, we did not see any difference between the placebo and active on the whole data set. When we look at those more relevant patients with the systemic inflammation, we see that after the first four weeks, the compound's effect really turns in, and we end up here with a higher, statistically significant, higher, fraction of the patients who qualified for this, MCID on active compared to placebo. And this more than 80% is high. In most literature when report this after 12 weeks is in this 70%, whereas the placebo here, or rather the placebo effect, very, very much mimic what we see on rituximab in the literature. So this is an encouraging, very, very encouraging finding, indicating the potential of the treatment with resomelagon in patients with activated systemic inflammation. When we then go to the clinical disease activity index, that's in the inclusion criteria for the patient, it should be about 22 in order to to be participating in the study. And the average in the patient population was around 40 in placebo and a little higher in the resomelagon group. And when we look at the patient population with CRP, the subpopulation, it was slightly higher than that. Again, if we look at the full patient population, we saw a numerically higher, but not that dramatic better reduction in CDAI at all time points in active versus placebo. And when we then go to the patients with the activated systemic inflammation, well, we see that this numerical changes between active and placebo is higher at all time points. Again, indicating that the compounds in this study here, in a study that was not designed to show statistical significance in a subpopulation as the one we have identified, is very, very encouraging. The last slide I would like to show you is another scoring system, the DAS28, which is widely used also as a registration readout in Europe for compounds for treatment of rheumatoid arthritis. The DAS28 scoring is based on where the CDAI scoring is based on tender and swollen joint, as well as patient and investigators' judgment of global disease activity. The DAS score is based on, again, the tender and swollen joints, but then also on the patient's assessment of disease activity, and then data, and the last point is changes in CRP. On the full dataset, we could not see any difference between the two groups. But as for the ACR, the HAQ, the DAS, the CDAI, in the patient population that activated systemic inflammation, we see a numerically higher reduction in DAS at the 12th, and the 8th and the 12th weeks time point. So all in all, based on these findings, and together with the what we reported last time, it's a very well-tolerated compound, we find this very, very encouraging and look very, very much forward, not only to get the results of the next study, but also to design study moving forward in this very relevant patient population, where the resolution therapy induced by resomelagon has a large potential. Thank you very much, Thomas. So what we have shown you today is really what we believe is a very relevant subpopulation. Of course, it is not more than about 60 or 61% of the total population, but this population, we can, with more clarity, say, do have a systemic beginning systemic inflammation. And treating with resomelagon, that is a anti-inflammatory drug, rebalancing the immune system, that is a relevant group of patients. As I said in the beginning, from a drug development point of view, what is reassuring here, and that is exactly what we saw in the BEGIN study as well, is to have all parameters pointing in the same direction. And that gives us belief that this is real, what we are seeing. This gives us a very good belief that we have a compound that is active and that is able to treat inflammatory diseases. As many of you remember, we have both the BEGIN positive data, we have the positive data in COVID-19-induced lung inflammation, and now we have this subpopulation of patients in the EXPAND study showing activity, I would say. What to expect next? If we take a Q3 top-line result from the EXPAND, of course, that we came out with a bit more than a week ago. Now, the sub-analysis from the EXPAND and secondary variables, you have seen all the data that we have so far. As Thomas said, we have an excellent safety profile. We need to remember that as well when we talk about the sub-analysis. In Q4, we are expecting the top-line result from part A in RESOLVE. As was in the press release yesterday and what Thomas said, we know that about 70% of these study subjects, the patients, do have CRP about three, so that is encouraging, of course. In addition to that, we are looking at DMARD IR patients. So these patients has been on methotrexate for quite some time, and it doesn't really work anymore. So these two parameters are giving us a cautious hope for that study. In addition to that, we will come with the mode of action study that we did in EXPAND, measuring different parameters on inflammation, getting a more grip around detailed how does resomelagon interact in the inflammation? And of course, with the data from today, this is encouraging to go in and look at those patients with increased CRP there as well. And, of course, we'll have more results from part A RESOLVE in Q4 as well. In the first half of next year, if data in RESOLVE are good, obviously, we would like to initiate the RESOLVE part B. And with the knowledge that we have today, I think that that would be quite encouraging. And then, of course, initiation of phase I, TXP-11, and of course, more pipeline updates. So we have a rich pipeline and a rich, potential good news flow, coming the next several quarters. So with that, I would like to open up for questions. If you wish to ask a question, please dial star five on your telephone keypad to enter the queue. If you wish to withdraw your question, please dial star five again on your telephone keypad. The next question comes from Gonzalo Artiach from ABG Sundal Collier. Please go ahead. Hi, and thank you for taking the questions. I have a couple of them. The first one, based on the data that you have provided, the ACR20 in patients with CRP below 3 mg/L should be 30%, and this number compares significantly lower to the placebo group at around 55%. So could you give us your view on that? I mean, why would be the addition of resomelagon be bad if CRP levels are below three? Thank you. Well, thank you. Let me answer that. It's Thomas here. You're right, that is a lot of consequence. What I think is the answer to this is that the compound, in order to work, should be able to induce its pharmacological effect with ongoing some degree of ongoing systemic inflammation. Whereas if you go in and treat, and it might be a dose question, in patients with very low circulating levels of CRP, and we have to dig further into understand the inflammatory response, it seems so that it might not be, or rather you should avoid to do that. And from mode of action of the compound, that actually makes a lot of sense. We know that it does not induce any effects with regard to immune system in healthy volunteers, and when we test that in different human samples, we also always have to challenge the samples in order to induce a pharmacological inflammatory response in order to show efficacy of the compound. So I think it's very much in line with what we would expect for a compound that has the ability to induce resolution. Okay, thank you. A second one, it's on the mechanism of action. So, I mean, in the resolution of inflammation, it's true that you need a certain degree of inflammation to be able to resolve it, let's say, but not necessarily it has to be systemic inflammation. I mean, it could also be local inflammation, like the one that you have in the joints Yeah. In patients with RA. So is there any. Well, I mean, this local inflammation is chronic, it's constant, it doesn't fluctuate. So is there any connection of this, of CRP, which fluctuates in between flares and the local environment at the joints? The answer would be that, we know that CRP is fluctuating and is, you could say, a measurement on a spillover of local inflammation go to systemic. So yes, when we then have. So, in other words, when you do have a CRP level that is above normal level, it's an indication of a systemic inflammation that goes beyond the local joint, the local tissue, in this case, the joint, or you could say a more severe inflammation. So one way, another way to say that would be, again, that in order to have a therapeutic effect of the compound, we need a certain level of inflammation, either systemically or locally. We have not been through all the readouts right now, but we do have measurements, and we'll come and look at that on the synovial inflammation. I wonder whether it would be so that those patients who have the indication of systemic inflammation also would be the one who responds to synovial modulation, simply because it's more avid in the inflammation more avid in these patients. Okay, and one last question from my side, if possible. Yeah. In the BEGIN study, you stated back in 2021 that you did not achieve statistical significance versus placebo in reducing the proportion of patients going from severe to moderate. Because, I mean, the reason you gave it was because of CRP levels being higher than the 100 milligrams. So this contradicts in a certain way what your new analysis does. So could you give us some color on this discrepancy? I agree with you. What you refer to is that even though that we saw a numerically higher reduction in CDAI score in the 100 milligram in the BEGIN study compared to placebo, and also the 50 milligram, that was the lower dose we tested there. We saw a large numerical response, but we did not see as many patients going from high disease activity to moderate or lower as we as in the 50-milligram group, and only slightly more than in placebo group. So that's right. But we also then had a higher starting level. So, I would say that if we look at the 100 milligram and the 50 milligrams together in that group, where the 50 milligram actually had more than 60% of the patient went from high disease activity to moderate disease activity or lower, there was a clear trend, but it was not clear-cut dose response as it was on most other readouts. And that might be so that one explanation could be that that had to do with CRP. But rather turn it the other way around, because when we now here have we looked at the data here in the EXPAND, and honestly, we have great difficulty to understand why we did not see a signal having the BEGIN study in mind. So I also went back to the BEGIN study, and we knew that if we had higher, the higher we go up in CRP, cutoff rate of six, or in this case, a cutoff rate of three, then the likelihood to have patients to respond on ACR20 are increased. So the signal was also there, but the number of patients who had very low disease activity with regard to, based on CRP was not as in this study, where actually 40% of them were present. So there is some kind of correlation that we need to understand further, and I firmly believe that we, moving forward, should avoid to give this compound to patients who do not have indication of systemic inflammation. So, Gonzalo, Torbjørn here. Hi. So, what we also saw in this study, in the study population, the sub-study population, was that when we looked at activity of resomelagon in the 100 mg group, of those, 83% of those patients having activity also had a CRP about three. So again, indicating, showing what Thomas is alluding to, CRP is a good marker for this type of treatment. Okay, right. Thank you very much. Thank you, Gonzalo. The next question comes from Carl Olsson from Celio AB. Please go ahead. Hello, I'm on the phone. Do you hear me? Yes, we hear you, Carl. Okay. I'm not in the business, principally, I'm an investor in general. Regarding the inflammation level, I have a question principle. Let's assume that the population in Europe between 1800 and 1900 was 38 degrees Celsius, something like that, and now the average temperature on the population after 1900, 2000 is approximately 37 degrees Celsius. Now, when it comes to the COVID-19, let's assume that if you have a lower temperature than your normal 37 degrees Celsius, if you are a person who having just 37 degrees Celsius as the average temperature, is your substance or product is it possible to bring it down, for instance, at 1 degree on such a person to be able to resist COVID-19 inflammation in a better way? I don't know if that is a far-out question, but, I would like to have your views in principle. I think I got it. What you should ask about is whether we, by promoting resolution, potentially then could make a, you could call it a left shift of the disease activity. You mentioned COVID-19 as an example. It could be other inflammatory diseases. It could be other infections. We believe in principle, yes, and what I think the data here shows and actually support very much is that if we do have a systemic inflammation, we can go in and modulate that. It was not the data set is very encouraging on this subset of patients that where we say we have this systemic ongoing inflammation, whereas on the full data set, we did not see what we had expected, and now we have to understand and build that moving forward. So that means that, let's assume for the next COVID-19 variants or a similar thing, maybe this could be some sort of a basic drug or substance that could help people to have a better recovery or influence on the virus itself during the sick period, so to say. Yes, Carl, Torbjørn here. Yes, absolutely, it could be an opportunity, because when we go back and look at the data we got in the RESOVIR and in the COVID-19 patients, we did find that they could come home much earlier, and they needed less oxygen treatment. So it was quite clear from what we saw at that point of time, that we could treat this broader severe inflammation in the lung. In addition to that, we saw a very fast onset to action. It was within days. So we are thinking about, you know, also including other viruses like the influenza. Influenza is definitely killing people all around the world every year. However, our focus today will be and is the rheumatoid arthritis to get the full picture of resomelagon in rheumatoid arthritis, and here we have the RESOLVE data coming, we have the mode of action data coming, and, as we have presented today, we believe that we have found a subpopulation of patients that are quite promising in terms of target population in the first line treatment of RA. Now, with the DMARD-IR patients in RESOLVE, we'll see if we can get a resensitization of those patients that does not respond anymore on the methotrexate. So we have very exciting time ahead of us. Okay. So thank you very much. It looks promising, and good luck. Thank you, Carl. Thank you. Bye. As a reminder, if you wish to ask a question, please dial star five on your telephone keypad. There are no more questions at this time, so I hand the conference back to the speakers for any closing comments. Dear everybody, thank you so much for your time today. We will put the presentation on our webpage, so you can digest it and analyze it, and you're so much welcome to get back to us with further questions that you might have. So Thomas and I, we say thank you so much for your time today. Thank you. Bye.